Sepsis / Septic Shock

Resuscitate before induction - Restore intravascular volume and start vasopressors (norepinephrine first-line) before or during induction; the vasodilated, underfilled patient can arrest on induction.

Choose a hemodynamically stable induction - Etomidate or reduced-dose ketamine preserve pressure better than a propofol bolus; give all agents slowly and in reduced doses.

Do not delay source control or antibiotics - Early antibiotics and source control take priority; coordinate timing with surgery.

Vasopressor and inotrope support - Norepinephrine, with vasopressin added as needed, and an inotrope for septic cardiomyopathy; use an arterial line and consider central access.

Ventilation and organ support - Use lung-protective ventilation given the ARDS risk, and anticipate coagulopathy or DIC, electrolyte and acid-base derangement, and relative adrenal insufficiency (consider stress-dose steroids).

Telling it apart from the other distributive shock - Septic and neurogenic shock are both warm and vasodilated, so the heart rate is what separates them. Septic shock is tachycardic; neurogenic shock from a cord injury above T6 is characteristically bradycardic, because the cardiac accelerators are cut off and vagal tone is unopposed. A warm, hypotensive, bradycardic trauma patient is not septic - see the Neurogenic Shock and Spinal Injury entry.

Perfusion endpoints, not just a pressure - Lactate above 2 mmol/L alongside a vasopressor requirement is what defines septic shock, so trend it rather than reading it once. Central venous oxygen saturation at or above 70 percent, base deficit, and urine output are the other markers of perfusion adequacy; a urine output under 0.5 mL/kg/hr signals renal hypoperfusion and is often the earliest sign that a patient is slipping.

What those numbers will not tell you - A normal blood pressure early does not exclude shock: the compensated patient can be warm, flash-refilling, and normotensive while already hypoperfusing. Physical exam alone is unreliable for identifying which shock you are dealing with. Pulse pressure variation is only valid as a fluid-responsiveness measure in a patient without spontaneous breaths or arrhythmias - it will mislead you in the spontaneously breathing patient or the one in AF.

Mixed and evolving shock - The four categories are not mutually exclusive and real patients sit in more than one. A septic patient who is also bleeding, or dry from days of poor intake, is distributive plus hypovolemic; add the myocardial depression and there is a cardiogenic component on top. Treat the component that dominates now and reassess after each intervention - a vasopressor does nothing for an unfilled ventricle, and volume alone will not hold a pressure against a resistance that has collapsed.

Life-threatening organ dysfunction caused by a dysregulated host response to infection. Septic shock is its most severe form - vasodilatory (distributive) hypotension requiring vasopressors, with an elevated lactate despite fluid resuscitation. The physiology is a combination of profound vasodilation, capillary leak with relative hypovolemia, myocardial depression (septic cardiomyopathy), coagulopathy, and evolving multi-organ dysfunction. Inducing anesthesia in this patient without preparation can precipitate cardiovascular collapse.

Where this sits among the shock states: shock sorts into four categories - distributive, hypovolemic, cardiogenic, and obstructive - and septic shock is the leading cause of the distributive group, which is itself the most common category overall. Reported mortality runs 40 to 50 percent. The hemodynamic fingerprint that separates it: systemic vascular resistance falls while cardiac output is preserved or high (a hyperdynamic state, with a dynamic precordium and bounding peripheral pulses), and filling pressures are low. That is the mirror image of hypovolemic and cardiogenic shock, where cardiac output drops and resistance climbs. Oxygen extraction is also abnormal in distributive shock, so a central venous oxygen saturation drawn from an SVC line can read normal or high while the tissue is still hypoxic.

The bedside picture changes with stage. Early "warm shock" is warm extremities, flash capillary refill under one second, and bounding pulses - and the blood pressure may still be normal. As catecholamines rise and flow is shunted away from gut, kidney, muscle, and skin, it becomes "cold shock": cool mottled extremities, capillary refill over three seconds, thready pulses, and by then hypotension is established.